Worm Breeder's Gazette 10(1): 23
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
In the last C. elegans Newsletter we reported on the isolation of EMS-induced extragenic suppressors of bli-6(mn4), a dominant mutation causing blister formation. Since the time of that report, one of us changed her name from Winter to Schuyler and left the laboratory for some months before returning to the worm-picking life in general and suppressors of bli-6 in particular. We noted in the last report that 23 of our suppressors by themselves result in a dumpy phenotype, and all of these mutations were assigned to known dpy genes (but mutations in some dumpy genes do not suppress bli-6(mn4)). Here we report some progress with those suppressors that do not confer a dumpy phenotype. We have assigned 16 independent wild-type suppressors to linkage groups: eleven to LGII, two to LGIV and three to X. Although some of the suppressors are dominant in the sense that animals of genotype sup/+; bli-6(mn4)/+ are non-Bli, in all cases sup/+; bli-6(mn4)/bli- 6( mn4) animals are Bli (sup/sup; bli-6(mn4)/bli-6(mn4) are non-Bli); therefore it is possible to conduct complementation tests among all pairs of suppressors. The three X-linked mutations appear to complement all other mutations except each other, but we have also seen several examples of noncomplementation of nonallelic mutations, as expected from the work of Kusch and Edgar (1986; Genetics 113: 621- 639). We have so far tentatively assigned three of the mutations to known genes, based on both complementation testing and map position. For example, the homozygous mn312 mutant is not a roller, but mn312/rol-8(sc15); bli-6(mn4) animals were non-Bli (and slight left rollers) and gave no Bli recombinants among 4,800 self progeny (rol-8( sc15) is a recessive suppressor of bli-6(mn4); by contrast rol-1(e91) and rol-6(e187) do not suppress). By similar arguments, we are assigning mn309 to dpy-10, despite the fact that by itself it does not confer a dumpy phenotype, and we are assigning at least one of the LGIV mutations to dpy-4.Kusch and Edgar (C. elegans Newsletter 9, no. 1) identified mutation called sc109 as a recessive suppressor of bli- 6(sc16). Curiously, sc109 does not suppress bli-6(mn4). (We've confirmed that our copy of sc109 does suppress sc16.) We do not know the null phenotype of bli-6. It does not seem to be wild type, since wild-type revertants of mn4 invariably carried extragenic suppressors. Revertants of mn4/+ have also not yet yielded anything but extragenic suppressors. We plan to identify deficiencies of bli-6(mn4), which we have mapped close to midway between unc-5 and unc-24.Many of the sup; bli-6(mn4) stocks show defects in alae, such as breaks in the ridges, as viewed by Nomarski microscopy. One type of disconnection in ridges seems to be unique to the X-linked mutations. The alae and annulae of bli-6(mn4) animals seem to be normal. We have seen some abnormalities in annulae of mutants by scanning electron microscopy.